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Low Molecular Weight Sulfated Chitosan: Neuroprotective Effect on Rotenone-Induced In Vitro Parkinson's Disease

机译:低分子量硫酸盐壳聚糖:对旋转环酮诱导的体外帕金森病的神经保护作用

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The present investigation was an attempt to study the effect of low molecular weight sulfated chitosan (LMWSC) on in vitro rotenone model of Parkinson's disease (PD) by evaluating cell viability, oxidative stress, mitochondrial membrane potential, DNA fragmentation, and apoptosis. Incubation of SH-SY5Y cells with 100nm rotenone resulted in neuronal cell death, redox imbalanced mitochondrial dysfunction, DNA fragmentation, condensation, and apoptotic cellular morphology. Rotenone exposure enhanced the expression of preapoptotic (cytochrome C (cyto c), caspase-3, -8, -9, and Bax) and down-regulated the expression of anti-apoptotic (Bcl-2) markers. Reduction of the intracellular reactive oxygen species (ROS) levels ensued due to pretreatment of LMWSC along with consequent normalization of antioxidant enzymes, mitigation of rotenone induced mitochondrial dysfunction and apoptosis. Our current findings suggested that LMWSC exhibit the pronounced neuroprotective effects, which could be due to its antioxidant, mitochondrial protection, and anti-apoptotic properties. We thus conclude that LMWSC could be developed as a novel therapeutic molecule for the benefit of reducing the consequences of PD. However, further extensive preclinical and clinical studies are warranted.
机译:本研究旨在通过评估细胞活力,氧化应激,线粒体膜电位,DNA碎片和细胞凋亡来研究低分子量硫酸壳聚糖(LMWSC)对帕金森病(PD)的体外旋转酮模型的影响。用100nm旋转环孵育Sh-Sy5Y细胞导致神经元细胞死亡,氧化还原不平衡线粒体功能障碍,DNA碎片,缩合和凋亡细胞形态。旋转龙曝光增强了预补孔(细胞色素C),Caspase-3,-8,-9和Bax的表达,下调了抗凋亡(Bcl-2)标记的表达。由于LMWSC的预处理,随后抗氧化酶的预处理,随后的抗氧化酶的标准化,减轻了旋转吲哚诱导的线粒体功能障碍和细胞凋亡,随后的细胞内活性氧物质(ROS)水平。我们目前的研究结果表明,LMWSC表现出明显的神经保护作用,这可能是由于其抗氧化剂,线粒体保护和抗凋亡性质。因此,我们得出结论,可以作为一种新的治疗分子来发展LMWSC,以减少PD的后果。然而,有必要进一步广泛的临床前和临床研究。

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